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AMACR staining was positively expressed in 86 of the prostate carcinoma cases and completely absent in remaining 12.
Data show a significant association between Alpha-methylacyl-CoA racemase (AMACR) and ERG (show ERG Proteins) protein with prognostic implication in prostate cancer.
AMACR is expressed in most of the chordomas but only in a minority of chondrosarcomas. AMACR may serve as IHC marker of chordoma with differentiating ability comparable to that of beta-catenin (show CTNNB1 Proteins).
AMACR transcripts were detected in all radical prostatectomy(RP)-prostate cancer and RP-Benign samples but not in non-cancerous cystoprostatectomy samples, which suggest a global increase of AMACR expression in cancerous prostates.
AMACRwas not regulated in the white blood cells of multiple sclerosis patients
study showed that 34betaE12 is the most appropriate negative marker to combine with alpha-methylacyl coenzyme A racemase as a positive marker for the diagnosis of prostate adenocarcinoma[34betaE12]
The D175G and M9V polymorphisms of the AMACR gene are related to prostate cancer. The S201L polymorphism might be linked with prostate cancer risk. no association was observed between K277E or Q239H polymorphisms and susceptibility to prostate cancer.
AMACR amplification is a mechanism driving increased mRNA and protein expression and conferring aggressiveness through heightened cell proliferation in gastrointestinal stromal tumors
In diagnosis of ovarian clear cell carcinoma, AMACR is highly specific but suboptimally sensitive.
Overexpressed AMACR in myxofibrosarcomas can be amplification-driven, associated with tumor aggressiveness, and may be relevant as a druggable target.
observed a disease-dependent elevation of AMACR expression in monocytes and T cells from blood, draining lymph nodes and spleen of autoimmune experimental encephalomyelitis mice during preclinical phase; in vitro analysis revealed proliferation of T cells was inhibited in AMACR KO mice, but T-cell polarization was switched toward a pathogenic state
Phytol causes primary failure in liver leading to death of Amacr-/- mice thus emphasizing the indispensable role of Amacr in detoxification of alpha-methyl-branched fatty acids.
AMACR has a role in the synthesis of bile acids.
Metabolic adaptation allows Amacr-deficient mice to remain symptom-free despite low levels of mature bile acids.
This gene encodes a racemase. The encoded enzyme interconverts pristanoyl-CoA and C27-bile acylCoAs between their (R)- and (S)-stereoisomers. The conversion to the (S)-stereoisomers is necessary for degradation of these substrates by peroxisomal beta-oxidation. Encoded proteins from this locus localize to both mitochondria and peroxisomes. Mutations in this gene may be associated with adult-onset sensorimotor neuropathy, pigmentary retinopathy, and adrenomyeloneuropathy due to defects in bile acid synthesis. Alternatively spliced transcript variants have been described. Read-through transcription also exists between this gene and the upstream neighboring C1QTNF3 (C1q and tumor necrosis factor related protein 3) gene.
, Alpha-methylacyl-CoA racemase
, alpha-methylacyl-CoA racemase-like
, amacr protein
, 2-methylacyl-CoA racemase
, 2-arylpropionyl-CoA epimerase
, alpha-methylacyl-Coenzyme A racemase